Abstract

Paclitaxel is a member of the taxane agents that has demonstrated efficacy in ovarian cancer, both in first- and in second-line therapy. Counted among the side-effects of this drug are neurological disorders. In the present study, a rare case of a non-neuropathic ocular disorder, known as cystoid macular edema (CME), due to paclitaxel in patients treated for ovarian cancer is described. Macular edema, or CME, is a common cause of visual impairment that has been classically demonstrated by fluorescein angiograms, showing capillary leakage. CME without fluorescein leakage is rare, and its most common causes are juvenile X-linked retinoschisis, Goldmann-Favre syndrome, and niacin toxicity. At the present time, the mechanism associated with the form of CME that does not exhibit any signs of fluorescein leakage has not been elucidated due to an absence of histopathological studies. Several mechanisms have been proposed, although it is considered to occur due to disruption of the normal blood-retinal barrier by molecules with a molecular weight lower than that of fluorescein, which leads to fluid accumulation in the intracellular space. It is well known that taxane agents cause fluid retention, represented by edema, weight gain, and third-space fluid collection (pericardial, pleural, ascites), and this appears to be associated with their cumulative dose. The present case study confirms that macular edema associated with paclitaxel use exhibits spontaneous resolution following discontinuation of the causative agent. Taxane-associated maculopathy has been scarcely reported in the literature, but the gynecological oncologist should be alert to its possible development, and an ophthalmologic evaluation should be offered to all patients using paclitaxel.

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Spectral domain optical coherence tomography images derived from the present case study. (A) Baseline: Macular edema with a CRT of 515 µm in the RE. (B) Baseline: Macular edema with a CRT of 584 µm in the LE. (C) At 40 days after the interruption of plaxitel systemic therapy, CRT decreased to 320 µm in the RE. (D) At 40 days after the interruption of plaxitel systemic therapy, CRT decreased to 391 µm in the LE. (E) Three months later, the CRT was 232 µm in the RE, with the restoration of macular shape. (F) Three months later, the CRT was 316 µm in the LE, with the restoration of macular shape. (G) Four months later, the CRT was 230 µm in the RE. (H) Four months later, the CRT was 227 µm in the LE. (I) Eight months later, the CRT was 235 µm in the RE, with a normal macula shape. (J) Eight months later, the CRT was 234 microns in the LE, with a normal macula shape. CRT, central retinal thickness; LE, left eye; RE, right eye.